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Casadesus and colleagues make a case that hormonal changes associated with the dysregulation of the hypothalamic-pituitary-gonadal (HPG) axis following menopause/andropause are implicated in the pathogenesis of Alzheimer's disease (AD). Experimental support for this postulate has come from studies demonstrating an increase in amyloid-β (Aβ) deposition following ovariectomy/castration. Because sex steroids and gonadotropins are both part of the HPG feedback loop, decrements in sex steroids result in a proportionate increase in gonadotropins. They provide a review of the basic science relevant to luteinizing hormone (LH) and its receptor as a background for considering LH regulation of cognitive behaviors and AD pathology. Results of their analyses suggest that marked increases in serum LH following menopause/andropause is a physiologically relevant signal that could increase Aβ secretion and deposition in the aging brain. Suppression of the age-related increase in serum gonadotropins using anti-gonadotropin agents, such as leuprolide, is proposed as a novel therapeutic strategy for AD.
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